Recombinant BCG exporting ESAT-6 confers enhanced protection against tuberculosis
By A. Pym, P. Brodin, L. Majlessi, R. Brosch, C. Demangel, Ann Williams, K. Griffiths, G. Marchal, C. Leclerc, S. Cole. Nature Medicine, 2003
690 citations recorded by the source corpus.
Subfields: Immunology, Infectious Diseases
View Paper: https://www.semanticscholar.org/paper/9fc48bbba8997b88642d0442f72237f944b51198
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In Immunology
Citations in the corpus
- Extracellular M. tuberculosis DNA Targets Bacteria for Autophagy by Activating the Host DNA-Sensing Pathway (2012, positive): “This is a key difference between M. tuberculosis and BCG, as mutants lacking ESX-1 are defective for replication within macrophages, are severely attenuated in animal models of infection, and fail to activate innate immunesignaling responses of macrophages (Guinn et al., 2004; Hsu et al., 2003; Stan”
- Type VII secretion — mycobacteria show the way (2007, background): “However, recent studies have provided evidence that there is an alternative protein-secretion system in Gram-positive bacteri”
- The success and failure of BCG — implications for a novel tuberculosis vaccine (2005, background): “Adding deleted genes back to BCG or increasing the expression of immunodominant genes might improve the effects of BCG vaccination, as suggested by studies in animal model”